It’s pretty much standard practice in cancer research to search for genes that could serve as leads for new tumor-fighting drugs. But Cigall Kadoch, a 29-year-old assistant professor of pediatric oncology at the Dana-Farber Cancer Institute (yes, that means she’s already on the tenure track at Harvard) is following a new lead for anti-cancer medicines: exploring the genes that regulate the molecular structure of DNA itself.
Kadoch will be on stage at the Forbes Under 30 Summit on October 21, as part of a panel on the future of medicine, called Tomorrow’s Medicine Today.
A quick review of basic biochemistry: DNA is a molecular ladder in which a code made of molecules called bases (adenine, thymine, cytosine, and guanine or A, T, G, C) create recipes for all of the proteins that make up every part of the body, as well as instructions for when to make them.
But as with a computer’s hard drive, the code isn’t all that matters. The physical structure that reads the code and translates it for the body matter, too.
This DNA-reading structure, called chromatin, is constantly being modified as a way of determining what bits of DNA code get read. And the chromatin remodeling complex, which makes these modifications, is itself controlled by genes written into the DNA.
Kadoch, as a graduate student at Stanford, found that genes related to a chromatin remodeling complex called BAF, were, when mutated, the cause of a rare pediatric cancer: synovial sarcoma, usually found around major joints. Approximately 800 new cases occur in the U.S. each year.
Now, she has a 12-person team in her Boston lab looking for new drugs targeted at BAF, which might help not only kids with synovial sarcoma but also other patients. Kadoch guesses that 25% of cancers might be caused in part by BAF-related mutations. “It’s an amazing thing going from leading your own efforts to leading with a whole group behind you,” she says.